PMID- 1372239
OWN - NLM
STAT- MEDLINE
DCOM- 19920422
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 130
IP  - 4
DP  - 1992 Apr
TI  - Interleukin-1 alpha and tumor necrosis factor-alpha differentially regulate 
      enkephalin, vasoactive intestinal polypeptide, neurotensin, and substance P 
      biosynthesis in chromaffin cells.
PG  - 2252-8
AB  - The pattern of expression of at least four neuropeptides contained in 
      adrenomedullary chromaffin cells is altered by exposure to the cytokines 
      interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF alpha), 
      alone or in combination with stimulation of other second messenger pathways. 
      Vasoactive intestinal polypeptide (VIP) was elevated 2- to 3-fold by 1 nM IL-1 
      alpha within 48 h of exposure, while neurotensin and substance P synthesis were 
      unaffected, and met-enkephalin levels were decreased 25-35%. Stimulation of VIP 
      and substance P biosynthesis by forskolin was markedly enhanced by IL-1 alpha, 
      while forskolin stimulation of enkephalin and neurotensin biosynthesis was 
      unaffected. IL-1 alpha amplified the effect of phorbol myristate acetate to 
      increase the VIP content of chromaffin cells, but antagonized phorbol 
      ester-induced elevation of neurotensin levels. TNF alpha also demonstrated a 
      neuropeptide-specific pattern of modulation of second-messenger effects on 
      chromaffin cell neuropeptide levels similar to those seen with IL-1 alpha. The 
      neuroendocrine actions of IL-1 alpha described above, unlike IL-1 action in the 
      immune system, do not appear to be mediated through IL-2 as this cytokine did not 
      affect VIP or enkephalin expression in the presence or absence of protein kinase 
      stimulation. Neither IL-1 alpha nor TNF alpha affected the calcium-coupled 
      stimulation of neuropeptide secretion and biosynthesis that occurs in response to 
      cell depolarization in these and other neuroendocrine cells in vitro and in vivo. 
      These data provide a functional demonstration of IL-1 and TNF receptors in 
      chromaffin cell cultures and suggest a physiological role for cytokine production 
      in the adrenal medulla. Since both the magnitude and direction of neuropeptide 
      synthesis modulation by IL-1 alpha and TNF alpha are highly peptide-specific, it 
      appears that these cytokines do not merely augment second messenger pathways that 
      affect neuropeptide synthesis, but potentially regulate the activity of factors 
      controlling the pattern of neuropeptide gene expression in chromaffin cells.
FAU - Eskay, R L
AU  - Eskay RL
AD  - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and 
      Alcoholism, National Institute of Mental Health, Bethesda, Maryland 20892.
FAU - Eiden, L E
AU  - Eiden LE
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 1F7A44V6OU (Colforsin)
RN  - 33507-63-0 (Substance P)
RN  - 37221-79-7 (Vasoactive Intestinal Peptide)
RN  - 39379-15-2 (Neurotensin)
RN  - 58569-55-4 (Enkephalin, Methionine)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - Cattle
MH  - Cells, Cultured
MH  - Chromaffin Granules/*metabolism
MH  - Colforsin/pharmacology
MH  - Enkephalin, Methionine/*biosynthesis
MH  - Interleukin-1/*pharmacology
MH  - Interleukin-2/biosynthesis
MH  - Neurotensin/*biosynthesis
MH  - Substance P/*biosynthesis
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Vasoactive Intestinal Peptide/*biosynthesis
EDAT- 1992/04/01 00:00
MHDA- 1992/04/01 00:01
CRDT- 1992/04/01 00:00
PHST- 1992/04/01 00:00 [pubmed]
PHST- 1992/04/01 00:01 [medline]
PHST- 1992/04/01 00:00 [entrez]
AID - 10.1210/endo.130.4.1372239 [doi]
PST - ppublish
SO  - Endocrinology. 1992 Apr;130(4):2252-8. doi: 10.1210/endo.130.4.1372239.